Epidemiological studies have demonstrated that increased cancer risk is associated with obesity, but the underlying mechanism remains poorly understood. We have recently developed a Drosophila model of obesity; raising Drosophila on a diet high in carbohydrates led to metabolic dysfunction including hyperglycemia, insulin-resistance and accumulation of fat. Feeding a high dietary sucrose to Ras/Src co- activated Drosophila cancer model developed aggressive tumor with emergent metastasis in a diet-dependent manner. The goal of this Application is to further utilize Drosophila as a useful in situ model to explore mechanistic link between diet-induced obesity and tumor progression.